English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

T-type Ca 2+  channel Ca v 3.1 promotes microvessel contraction ex vivo. It was hypothesized that in vivo, functional deletion of Ca v 3.1, but not Ca v 3.2, protects mice against angiotensin II (ANG II)-induced hypertension. Mean arterial blood pressure (MAP) and heart rate were measured continuously with chronically indwelling catheters during infusion of ANG II (30 ng·kg −1 ·min −1 , 7 days) in wild-type (WT), Ca v 3.1 −/− , and Ca v 3.2 −/−  mice. Plasma aldosterone and renin concentrations were measured by radioimmunoassays. In a separate series, WT mice were infused with ANG II (100 ng·kg −1 ·min −1 ) with and without the mineralocorticoid receptor blocker canrenoate. Ca v 3.1 −/−  and Ca v 3.2 −/−  mice exhibited no baseline difference in MAP compared with WT mice, but day-night variation was blunted in both Ca v 3.1 and Ca v 3.2 −/−  mice. ANG II increased significantly MAP in WT, Ca v 3.1 −/− , and Ca v 3.2 −/−  mice with no differences between genotypes. Heart rate was significantly lower in Ca v 3.1 −/−  and Ca v 3.2 −/−  mice compared with control mice. After ANG II infusion, plasma aldosterone concentration was significantly lower in Ca v 3.1 −/−  compared with Ca v 3.2 −/−  mice. In response to ANG II, fibrosis was observed in heart sections from both WT and Ca v 3.1 −/−  mice and while cardiac atrial natriuretic peptide mRNA was similar, the brain natriuretic peptide mRNA increase was mitigated in Ca v 3.1 −/−  mice ANG II at 100 ng/kg yielded elevated pressure and an increased heart weight-to-body weight ratio in WT mice. Cardiac hypertrophy, but not hypertension, was prevented by the mineralocorticoid receptor blocker canrenoate. In conclusion, T-type channels Ca v 3.1and Ca v 3.2 do not contribute to baseline blood pressure levels and ANG II-induced hypertension. Ca v 3.1, but not Ca v 3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension.

american journal of physiology. renal physiology./american journal of physiology. renal physiology

Deficiency of T-type Ca2+ channels Cav3.1 and Cav3.2 has no effect on angiotensin II-induced hypertension but differential effect on plasma aldosterone in mice